Friedman J E, Lemon P W, Finkelstein J A
Applied Physiology Research Laboratory, Kent State University 44242.
J Appl Physiol (1985). 1990 Oct;69(4):1347-52. doi: 10.1152/jappl.1990.69.4.1347.
The genetically obese Zucker rat has a reduced capacity to deposit dietary protein in skeletal muscle. To determine whether amino acid uptake by muscle of obese Zucker rats is impaired, soleus strip (SOL) and epitrochlearis (EPI) muscles from 10-wk-old lean and obese Zucker rats were studied in vitro by use of [14C]alpha-aminoisobutyric acid (AIB). Muscles from fasted rats were incubated under basal conditions at rest or after a 1-h treadmill run at 8% grade. To equate total work completed, lean and obese rats ran at 27 and 20 m/min, respectively. Muscles were pinned at resting length, preincubated for 30 min at 37 degrees C in Krebs-Ringer bicarbonate buffer containing 5 mM glucose under 95% O2-5% CO2, and then incubated up to 3 h in Krebs-Ringer bicarbonate with 0.5 mM AIB, [14C]AIB, and [3H]inulin as a marker of extracellular fluid. Basal AIB uptake in EPI and SOL from obese rats was significantly reduced by 40 and 30% (P less than 0.01), respectively, compared with lean rats. For both lean and obese rats, exercise increased (P less than 0.05) basal AIB uptake in EPI and SOL, but the relative increases were greater in the obese rats (EPI 54% and SOL 71% vs. EPI 32% and SOL 37%). These results demonstrate that genetically obese Zucker rats have reduced basal skeletal muscle amino acid uptake and suggest that physical inactivity may partially contribute to this defect.
遗传性肥胖的Zucker大鼠在骨骼肌中沉积膳食蛋白质的能力降低。为了确定肥胖Zucker大鼠肌肉对氨基酸的摄取是否受损,我们使用[14C]α-氨基异丁酸(AIB)对10周龄瘦型和肥胖Zucker大鼠的比目鱼肌条(SOL)和肱三头肌(EPI)进行了体外研究。将禁食大鼠的肌肉在基础条件下于静息状态或在8%坡度的跑步机上跑1小时后进行孵育。为了使完成的总功相等,瘦型和肥胖大鼠分别以27和20米/分钟的速度奔跑。将肌肉固定在静息长度,在含有5 mM葡萄糖的Krebs-Ringer碳酸氢盐缓冲液中于37℃预孵育30分钟,95% O2-5% CO2条件下,然后在含有0.5 mM AIB、[14C]AIB和[3H]菊粉(作为细胞外液标记物)的Krebs-Ringer碳酸氢盐中孵育长达3小时。与瘦型大鼠相比,肥胖大鼠EPI和SOL的基础AIB摄取分别显著降低了40%和30%(P < 0.01)。对于瘦型和肥胖大鼠,运动均增加了(P < 0.05)EPI和SOL的基础AIB摄取,但肥胖大鼠的相对增加幅度更大(EPI为54%,SOL为71%,而瘦型大鼠EPI为32%,SOL为37%)。这些结果表明,遗传性肥胖的Zucker大鼠基础骨骼肌氨基酸摄取减少,提示身体活动不足可能部分导致了这一缺陷。